The role of TGF-β in polycystic ovary syndrome

Nazia Raja-Khan*, Margrit Urbanek, Raymond J. Rodgers, Richard S. Legro

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

81 Scopus citations


Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by chronic oligoanovulation and hyperandrogenism and associated with insulin resistance, type 2 diabetes, and cardiovascular risk. In recent years, genetic studies have linked PCOS to a dinucleotide marker D19S884 in the fibrillin 3 gene. Fibrillins make up the major component of microfibrils in the extracellular matrix (ECM) and interact with molecules in the ECM to regulate transforming growth factor β (TGF-β) signaling. Therefore, variations in fibrillin 3 and subsequent dysregulation of TGF-β may contribute to the pathogenesis of PCOS. Here, we review the evidence from genetic studies supporting the role of TGF-β in PCOS and describe how TGF-β dysregulation may contribute to (1) the fetal origins of PCOS, (2) reproductive abnormalities in PCOS, and (3) cardiovascular and metabolic abnormalities in PCOS.

Original languageEnglish (US)
Pages (from-to)20-31
Number of pages12
JournalReproductive Sciences
Issue number1
StatePublished - Jan 2014


  • TGF-β
  • fetal origins
  • fibrillin
  • genetics
  • polycystic ovary syndrome

ASJC Scopus subject areas

  • Obstetrics and Gynecology


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